Search PubMed⌕ Search

Biomedical subjects

J Lu

Publications and source records attributed to J Lu.

At least 415 records · Page 23Linked to original sources
PubMed1997

Mechanism of enhancement of esophageal tumorigenesis by 6-phenylhexyl isothiocyanate.

6-Phenylhexyl isothiocyanate (PHITC) enhances esophageal tumorigenesis induced by the carcinogen N-nitrosomethylbenzylamine (NMBA) in rats while its shorter chain analog, phenethyl isothiocyanate (PEITC), inhibits NMBA-induced esophageal tumorigenesis. A significant increase in O6-methylguanine levels in esophageal DNA at 72 h after NMBA administration to rats pretreated with PHITC suggested that PHITC might enhance NMBA metabolic activation or inhibit DNA repair. To test this hypothesis, groups of 20 rats were administered PEITC or PHITC at concentrations of 0, 1.0, or 2.5 mmol/kg in modified AIN-76A diet for 2 weeks. The esophagi were removed from rats, stripped, split, and maintained in HEPES buffered saline (HBS) for assays of NMBA metabolism (n = 5 per group) or were snap frozen for DNA repair assays (n = 15 per group). The principal metabolites of NMBA produced by esophageal explants were: two unidentified peaks, benzyl alcohol (at 4 h only), and benzoic acid. Esophageal explants from PEITC-treated animals showed a significantly decreased ability to metabolize NMBA as expected. PHITC-treated animals showed a slight inhibition in the formation of most NMBA-related metabolites, rather than an overall increase in NMBA activation. This inhibition was less than that observed with PEITC. No inhibitory effects were observed on O6-alkylguanine transferase (AGT) activity in the esophagi of rats treated with 1.0 micromol/g or 2.5 micromol/g PHITC. Thus, effects of PHITC on esophageal metabolism and DNA repair do not account for the enhancement of NMBA tumorigenicity by PHITC.

Animals↗
PubMed1997

Sulfone metabolite of sulindac inhibits mammary carcinogenesis.

Sulindac sulfoxide, a commonly prescribed anti-inflammatory drug, has cancer chemopreventive activity. During its metabolism, the inactive prodrug sulindac sulfoxide undergoes either reduction to the active anti-inflammatory metabolite sulindac sulfide or irreversible oxidation to sulindac sulfone, which lacks prostaglandin synthetase inhibitory activity. Interestingly, sulindac sulfone has been reported to have cancer chemopreventive activity. The objective of the experiments reported here was to investigate the chemopreventive activity of sulindac sulfone against mammary carcinogenesis and to study its mechanism. Rats were injected with either 12.5 or 37.5 mg of 1-methyl-1-nitrosourea (MNU)/kg body weight at 50 days of age. Sulindac sulfone was incorporated into a purified diet at a concentration of either 0.03 or 0.06% (w/w) and fed to rats beginning 7 days after the injection of MNU. Sulindac sulfoxide at a level of 0.06% (w/w) was fed as a reference for comparison. Thirty rats were assigned to each dietary group treated with the high dose of MNU, and 44 rats were assigned to each dietary group treated with the low dose of MNU. The sulfone reduced cancer incidence and the number of cancers per rat irrespective of the dose of MNU injected, and its chemopreventive activity was comparable to that of sulindac sulfoxide. Cancer latency was also prolonged significantly by sulindac sulfone; the effect was particularly notable at the low dose of carcinogen, at which the prolongation of latency was >8 weeks. The sulfone inhibited the occurrence of mammary carcinomas that were classified as having either a wild-type or a mutant codon 12 in the Ha-ras gene; however, the inhibitory effect was greater against carcinomas with a mutant Ha-ras genotype. Using a mammary gland organ culture transformation assay, it was observed that sulindac sulfone also inhibited the formation of 7,12-dimethylbenz(a)anthracene-induced hyperplastic alveolar nodules and that the inhibitory activity of the sulfone was comparable to that of the sulfoxide. These data indicate that the observed effect of the sulfone on mammary carcinogenesis in vivo is likely to be due to a tissue-specific effect rather than to other systemic effects. The findings that both the prodrug and the sulfone inhibited carcinogenesis in vivo and nodule formation in organ culture and that the sulfone lacks inhibitory activity on prostaglandin synthesis suggest a mechanism(s) of chemoprevention that is independent of the prostaglandin pathway. A candidate mechanism for the apparent clonal selection pressure exerted by the sulfone against mammary carcinogenesis is apoptosis. To test this hypothesis, MCF-7 cells were exposed to a range of concentrations of sulindac sulfone and sulfoxide. Both compounds inhibited cell growth and induced apoptosis in the absence of necrosis. Collectively, these data support a specific chemopreventive effect of sulindac sulfone against mammary carcinogenesis and indicate that this compound may have a selective effect against carcinogenesis involving alterations in the signal transduction cascade of which Ha-ras is a component. Evidence is consistent with the involvement of apoptosis in the cancer-inhibitory activity observed.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

A retrospective quality of life analysis using the Lung Cancer Symptom Scale in patients treated with palliative radiotherapy for advanced nonsmall cell lung cancer.

PURPOSE: To measure symptom palliation in patients treated with radiation therapy for advanced nonsmall cell lung cancer (NSCLC). METHODS AND MATERIALS: Five hundred thirty patients with NSCLC were treated at the Medical College of Virginia between 1988 and 1993. Sixty-three patients with the least favorable prognostic features received palliative radiation to 30 Gy in 10 or 12 fractions for symptoms related to the presence of intrathoracic tumor. The observer portion of the Lung Cancer Symptom Scale (LCSS) was employed in a retrospective chart review, scoring measures of appetite, fatigue, cough, dyspnea, hemoptysis, and pain. RESULTS: In 54 evaluable patients, median survival was 4 months and was independent of age, stage, performance status, or histology. Ninety-six percent of the patients had at least one LCSS symptom at presentation. Fatigue was unaffected by therapy. Improvements in appetite (p = 0.68) and pain (p = 0.61) were not statistically significant. There was, however, a statistically significant reduction in cough (p = 0.01), hemoptysis (p = 0.001), and dyspnea (p = 0.0003). Self-limiting acute side effects included transient esophagitis in 37% of patients, though no severe toxicities were noted. CONCLUSIONS: These results suggest symptomatic benefit from radiotherapy even in those NSCLC patients with advanced disease and a limited life expectancy. Treatment should be given to patients whose symptoms are most amenable to palliation. A site-specific quality of life instrument such as the LCSS should be included within any future clinical trial of NSCLC management so that symptom control may be scored as a treatment outcome in addition to disease-free survival.

Aged↗
PubMed1997

Gene expression changes associated with chemically induced rat mammary carcinogenesis.

Experimentally induced models of breast carcinogenesis in the rat are widely used for studying the biology of breast cancer and for developing and evaluating cancer prevention and control strategies. However, very little is known about gene expression changes that are associated with experimentally induced mammary carcinogenesis. This paper reports the identification, by differential display of mRNA and molecular cloning, of seven cDNA fragments of gene transcripts overexpressed in mammary carcinomas induced by 1-methyl-1-nitrosourea. These genes included the rat homologues of human galectin-7 gene, the human/mouse melanoma inhibitory activity/bovine chondrocyte-derived retinoic acid sensitive protein gene, the mouse stearoyl-CoA desaturase-2 gene, and the mouse endo B cytokeratin/human cytokeratin-18 gene. Although each of these genes has been implicated in some aspect of carcinogenesis in other organs, this paper is the first report of their overexpression in chemically induced mammary carcinomas. Two previously uncharacterized gene transcripts were also identified. A comparison of the expression levels of several genes in mammary carcinomas with those in the normal mammary gland tissue of virgin rats, mid-stage pregnant rats, and of day 1 postpartum lactating dams indicated that the overexpression of several genes observed in mammary carcinomas could not be accounted for by either a difference in the mammary epithelial content between mammary carcinoma and normal mammary tissue or by mammary epithelium-specific proliferation associated with pregnancy. Several genes were also overexpressed in rat mammary carcinomas induced by 7,12-dimethylbenz[a]anthracene but not in azoxymethane-induced rat colon adenocarcinomas. The genes identified in this study may therefore represent mammary carcinoma-specific molecular markers that may be helpful in investigations of mammary carcinogenesis and its prevention.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

Collectins: collectors of microorganisms for the innate immune system.

Collectins are a group of multimeric proteins mostly consisting of 9-18 polypeptides organised into either 'bundle-of-tulips' or 'X-like' overall structures. Each polypeptide contains a short N-terminal segment followed by a collagen-like sequence and then by a C-terminal lectin domain. A collectin molecule is assembled from identical or very similar polypeptides by disulphide bonds at the N-terminal segment, formation of triple helices in the collagen-like region and clusters of three lectin domains at the peripheral ends of triple helices. These proteins can bind to sugar residues on microorganisms via the peripheral lectin domains and subsequently interact, via the collagen-like triple-helices, with receptor(s) on phagocytes and/or the complement system to bring about the killing and clearance of the targets without the involvement of antibodies. The collectins can also bind to phagocyte receptor(s) to enhance phagocytosis mediated by other phagocytic receptors. Lack, or low levels, of collectin expression can lead to higher susceptibility to infections, especially during childhood when specific immunity has not fully developed. Therefore, the collectins play important roles in the enhancement of innate immunity.

Animals↗
PubMed1997

Liver injury model induced in mice by a cellular immunologic mechanism--study for use in immunopharmacological evaluations.

Various drugs for clinical hepatitis were applied to a new model of liver injury induced in mice by delayed-type hypersensitivity to picryl chloride (PCI-DTH). The hepatoprotective agent, biphenyl dimethyl dicarboxylate showed a remarkable improvement against the elevation of serum transaminase levels as well as the histopathological changes when given during the induction phase but not during the effector phase of DTH reaction. Cyclophosphamide (Cy), an immunosuppressive agent, significantly inhibited the enzymatic elevation given in both induction and effector phases. However, Cy did not affect the sustaining of liver injury 4 weeks after the liver injury eliciting. Moreover, the consecutive administration of prednisolone (Pred), in both induction phase and sustaining process of liver injury, conversely caused a more severe liver damage. Such exacerbation by Pred might be resulted from its toxic action to hepatocytes. As an immunomodulatory and antiinflammatory agent, glycyrrhizin remarkably improved the sustaining process but not the acute phase of the liver injury. Krestin and malotilate also showed an improving effect on the sustaining development of liver injury. These findings that most of above drugs showed an improving action in their respective manner suggest that this model may be useful for the pharmacological evaluation of drugs especially immunomodulating agents for hepatitis.

Acute Disease↗
PubMed1997

Anti-inflammatory activity of the aqueous extract from Rhizoma smilacis glabrae.

Our previous paper has reported that the aqueous extract from Rhizoma smilacis glabrae (RSG) (RSG ext) selectively inhibited the effector phase of delayed-type hypersensitivity (DTH) without suppressing humoral immune response. In the present study, a remarkable inhibitory activity was exhibited by the extract against both primary and secondary hind paw swelling of adjuvant arthritis in rats. RSG ext also significantly reduced the inflammatory edema induced by carrageenan in either naive or bilaterally adrenalectomized rats, suggesting the independence of the anti-inflammatory action on the function of pituitary-adrenal axis. The PGE2 content in the carrageenan-induced inflammatory tissue was also decreased remarkably by the extract. Furthermore, RSG ext showed a distinct inhibition on the formation of cotton-induced granuloma formation. However, as compared with a steroidal agent, prednisolone, the extract did not affect the vitamin C content in adrenal gland as well as the weights of some organs. These results suggest that RSG ext may act as a therapeutic agent of immunoinflammatory diseases through a selective suppression on the cellular immune response involved in inflammations as well as through a direct anti-inflammatory mechanism including inhibiting PGE2.

Adrenal Glands↗
PubMed1997

A new strategy for regulating the immunological liver injury--effectiveness of DTH-inhibiting agents on DTH-induced liver injury to picryl chloride.

Aqueous extracts from various crude drugs showing a selective inhibition on the induction or effector phase of delayed-type hypersensitivity (DTH) reaction were applied to the new model of liver injury induced in mice by picryl chloride(PCl)-induced DTH. The inhibiting drugs to the induction phase of DTH, Fructus Triburi (FT) and Er-Miao-San (EMS), showed a remarkable improvement against the elevation in serum transaminase levels as well as in histopathological changes when given during this phase. The administration in the effector phase by Rhizoma Smilacis Glabrae (RSG) and Cortex Dictamni (CD), selectively inhibiting the phase of DTH, also significantly improved the liver damage. In addition, RSG and CD showed an almost complete recovery of serum alkaline phosphatase from a persistent decrease in the sustaining process of liver injury when given consecutively for 4 weeks after the elicitation of liver injury. Cyclophosphamide, an immunosuppressive agent, significantly inhibited the enzymatic elevation given in either phase, while it did not affect the ability to sustain liver injury. When the above extracts were given in a combined manner to the same mouse during these two phases, respectively, FT with RSG and EMS with CD showed a distinct synergism against the liver injury. RSG or CD also enhanced the activity of prednisolone in suppressing PCl-induced ear contact sensitivity. These findings suggest that this immunological liver injury may be regulated by a set of selective suppressants to DTH reaction and the suitable application of such agents may pave the way for a new strategy in treating liver damage.

Animals↗
PubMed1997

Anatomic considerations of the principal nutrient foramen and artery on internal surface of the ilium.

Direct measurements of the nutrient foramen of thirty dried ilia using digital calipers and observations of the nutrient a. from ten cadaveric specimens were made in the present study. The nutrient foramen was situated 12.5 +/- 2.7 mm lateral to the anterosuperior sacroiliac joint line but perpendicular to this line and 23.5 +/- 5.8 mm above the pelvic brim parallel to the sacroiliac joint line. The nutrient a. originated from the iliolumbar a. as it coursed across the anterosuperior aspect of the sacroiliac joint. The present anatomic study indicates that the nutrient a. on the internal surface of the ilium is prone to injury as a result of traumatic disruption of the sacroiliac joint, sacral alar fractures and during the anterior approach to the sacroiliac joint.

Aged↗
PubMed1997

Anatomic considerations of the second sacral vertebra and dorsal screw placement.

Direct measurements and measurements from images of axial cross-sections on 20 cadaveric sacra that had been scanned on computer were used in this study. The measurements, including parameters from the vertebral body, lateral mass and spinal canal of the second sacral vertebra (S2) were performed. The length of the screw path and the optimal angulation of the screw placement for dorsal sacral internal fixation were also included. The mean values of height, anteroposterior diameter, width and breadth of the S2 were 25.0 mm, 13.5 mm, 29.4 mm and 83.0 mm, respectively. The mean values of the mid-sagittal diameter, maximum transverse diameter and area of the S2 spinal canal were 10.3 mm, 23.1 mm and 162.4 mm2, respectively. The mean transpedicular screw length of the S2 and optimal medial angle were 25.2 mm and 30.0 degrees, respectively. The mean lateral mass screw length of the S2 and optimal lateral angle were 32.8 mm and 22.0 degrees, respectively. The present study provides quantitative anatomic data of the second sacral vertebra. All parameters indicate that, compared with our previous study, S2 is smaller than S1. When S2 lateral mass screw fixation is intended, anchoring the anterior cortex may violate the iliac vessels or lumbosacral trunk; therefore, understanding the unique anatomy of the S2 is imperative.

Aged↗
PubMed1997

Molecular motions of a glycopeptide from human serum transferrin studied by 13C nuclear magnetic resonance.

The molecular motions of a 21-amino-acid glycopeptide (Gp21) containing multiple glycoforms of an N-linked diantennary oligosaccharide were studied by two-dimensional 1H-detected 13C relaxation measurements at natural abundance. Gp21 was derived from human serum transferrin, its amino acid sequence is QQQHLFGSNVTDCSGNFCLFR, and its N-glycan structure is [Formula: see text] The measured longitudinal and transverse relaxation rate constants and the nuclear Overhauser enhancements for the methine carbons of Gp21 were analyzed by using the model-free approach to obtain information about the internal motions in the molecule. The calculated order parameters S2 of the alpha carbons in both NH2- and COOH-terminal segments of the peptide are smaller than those in the interior segment of the Gp21 peptide moiety, implying that the internal motions in the terminal segments are less restricted than in the interior segment. The average S2 value is 0.72-0.91 for the glycosyl residues in the pentasaccharide core of Gp21, 0.58-0.59 for the interior GlcNAc-5,5' residues in the two branches, and 0.35-0.51 for the terminal GlcNAc-5, Gal-6,6', and NeuAcN,N' residues in the two branches, indicating that the internal motions in the glycan core are more restricted than in the two branches.

Amino Acid Sequence↗
PubMed1997

One-shot delayed-type hypersensitivity reaction in the mouse liver causes a sustained liver injury to picryl chloride.

The developmental characteristics of liver injury induced by a delayed-type hypersensitivity (DTH) mechanism against picryl chloride were examined for 9 consecutive weeks in 3 mouse strains, BALB/c, Kunming and ICR mice. The changes of most biochemical parameters were similar in these three strains, namely, the activities of serum transaminases, lactic dehydrogenase, and prolidase were elevated significantly on day 1, during the first several weeks, and almost throughout the duration, respectively, of liver injury. The content of liver hydroxyproline was also increased after 1-9 weeks of liver injury. In addition, a significant decrease of liver weight, serum alkaline phosphatase and albumin level was observed in BALB/c and Kunming mice. Similar changes in liver histology were also found in the three strains. The hepatocellular necrosis and inflammatory infiltration into the portal area were the predominant features on day 1 and were still distinct during the subsequent several weeks. The mild or moderate hepatocellular degeneration, regeneration and connective tissue hyperplasia were observed after 1 or 3 weeks. A bridging necrosis between portal and portal was observed in several BALB/c and ICR mice, reflecting the possibility of exacerbation of liver injury. These results suggest that the liver injury could be caused and sustained by a one-shot DTH reaction to picryl chloride. The chronicity of the biochemical and histopathological characteristics may be helpful in elucidating the mechanisms of chronic development of liver injury.

Animals↗
PubMed1997

The inhibition of nitric oxide-activated poly(ADP-ribose) synthetase attenuates transsynaptic alteration of spinal cord dorsal horn neurons and neuropathic pain in the rat.

Transsynaptic alteration of spinal cord dorsal horn neurons characterized by hyperchromatosis of cytoplasm and nucleoplasm (so-called 'dark' neurons) occurs in a rat model of neuropathic pain induced by chronic constriction injury (CCI) of the common sciatic nerve. The incidence of dark neurons in CCI rats has been proposed to be mediated by glutamate-induced neurotoxicity. In the present study, we examined whether the inhibition of the nitric oxide (NO)-activated poly(ADP-ribose) synthetase (PARS), a nuclear enzyme critical to glutamate-induced neurotoxicity, would both reduce the incidence of dark neurons and attenuate behavioral manifestations of neuropathic pain in CCI rats. Dark neurons were observed bilaterally (with ipsilateral predominance) within the spinal cord dorsal horn, particularly in laminae I-II, of rats 8 days after unilateral sciatic nerve ligation as compared to sham operated rats. The number of dark neurons in the dorsal horn was dose-dependently reduced in CCI rats receiving once daily intrathecal (i.t.) treatment with the PARS inhibitor benzamide (200 or 400 nmol, but not 100 nmol benzamide or saline) for 7 days. Consistent with the histological improvement, thermal hyperalgesia, mechanical hyperalgesia, and low threshold mechano-allodynia also were reliably reduced in CCI rats treated with either 200 or 400 nmol benzamide. Neither dark neurons nor neuropathic pain behaviors were reliably affected by i.t. administration of either 800 nmol novobiocin (a mono(ADP-ribose) synthetase) or 800 nmol benzoic acid (the backbone structure of benzamide), indicating a selective effect of benzamide. Intrathecal treatment with an NO synthase inhibitor NG-nitro-L-arginine methyl ester (40 nmol, but not its inactive D-isomer) utilizing the same benzamide treatment regimen resulted in similar reductions of both dark neurons and neuropathic pain behaviors in CCI rats. These results provide, for the first time, in vivo evidence indicating that benzamide is neuroprotective and that the PARS-mediated transsynaptic alteration of spinal cord dorsal horn neurons contributes to behavioral manifestations of neuropathic pain in CCI rats. These observations may have general implications beyond treatment of neuropathic pain in that PARS-mediated neuronal alterations may play a significant role in glutamate-mediated neurotoxicity under many other circumstances.

ADP Ribose Transferases↗
PubMed1997

Binding of vanadate to human erythrocyte ghosts and subsequent events.

Spectroscopic techniques were used to investigate the interaction between vanadate and human erythrocyte ghosts. Direct evidence from 51 V nuclear magnetic resonance (NMR) studies suggested that the monomeric and polymeric vanadate species may bind to the anion binding sites of band 3 protein of the erythrocyte membrane. The results of 51V NMR studies and the quenching effect of vanadate on the intrinsic fluorescence of the membrane proteins indicated that in the low concentration range of vanadate (< 0.6 mM), monomeric vanadate binds mostly to the anion sites of band 3 protein with the dissociation constant close to 0.23 mM. The experiments of sulfhydryl content titration by the method of Ellman and residue sulfhydryl-labeled fluorescence spectroscopies clearly displayed that vanadate reacts directly with sulfhydryl groups. The appearance of the anisotropic election spin resonance (ESR) signal of vanadyl suggests that a small (c.3%) amount of vanadate was reduced by sulfhydryl groups of membrane proteins. The fluidity and order of intact ghost membrane were reduced by the reaction with vanadate, as shown by the ESR studies employing the protein- and lipid-specific spin labels. It was concluded that although vanadates mainly bind to band 3 protein, a minor part of vanadate may oxidize the residue sulfhydryl groups of membrane proteins, and thus decrease the fluidity of erythrocyte membrane.

Anion Exchange Protein 1, Erythrocyte↗
PubMed1997

Glycine68 to histidine73 has an important role in the function of human tumor necrosis factor alpha.

Mutant human tumor necrosis factor alpha(hTNF alpha) genes have been constructed by in vitro mutagenesis and expressed in Escherichia coli. A deletion involving Gly68 to His73 in hTNF alpha remarkably decreased the solubility and biological activity of hTNF alpha. From the above and results of a molecular dynamics simulation it is proposed that the region of Gly68 to His73 in hTNF alpha has an important role in the maintenance of the 3-D structure and modulation of the biological activity of hTNF alpha.

Amino Acid Sequence↗
PubMed1997

Identification of the binding site in intercellular adhesion molecule 1 for its receptor, leukocyte function-associated antigen 1.

Intercellular adhesion molecule 1 (ICAM-1, CD54) is a member of the Ig superfamily and is a counterreceptor for the beta 2 integrins: lymphocyte function-associated antigen 1 (LFA-1, CD11a/CD18), complement receptor 1 (MAC-1, CD11b/CD18), and p150,95 (CD11c/CD18). Binding of ICAM-1 to these receptors mediates leukocyte-adhesive functions in immune and inflammatory responses. In this report, we describe a cell-free assay using purified recombinant extracellular domains of LFA-1 and a dimeric immunoadhesin of ICAM-1. The binding of recombinant secreted LFA-1 to ICAM-1 is divalent cation dependent (Mg2+ and Mn2+ promote binding) and sensitive to inhibition by antibodies that block LFA-1-mediated cell adhesion, indicating that its conformation mimics that of LFA-1 on activated lymphocytes. We describe six novel anti-ICAM-1 monoclonal antibodies, two of which are function blocking. Thirty-five point mutants of the ICAM-1 immunoadhesin were generated and residues important for binding of monoclonal antibodies and purified LFA-1 were identified. Nineteen of these mutants bind recombinant LFA-1 equivalently to wild type. Sixteen mutants show a 66-2500-fold decrease in LFA-1 binding yet, with few exceptions, retain binding to the monoclonal antibodies. These mutants, along with modeling studies, define the LFA-1 binding site on ICAM-1 as residues E34, K39, M64, Y66, N68, and Q73, that are predicted to lie on the CDFG beta-sheet of the Ig fold. The mutant G32A also abrogates binding to LFA-1 while retaining binding to all of the antibodies, possibly indicating a direct interaction of this residue with LFA-1. These data have allowed the generation of a highly refined model of the LFA-1 binding site of ICAM-1.

Animals↗
PubMed1997

Screw placement in the lumbar vertebral isthmus.

Anatomic parameters of the isthmus from L1 to L5 were measured in 30 dried lumbar spines. All measured parameters were fairly constant from L1 to L5. The mean values of the core length, thickness of the superior and inferior borders of the isthmus, superoinferior diameter and posterior and medial inclinations of the lumbar isthmus at L5 were 39.9 +/- 2.3 mm, 2.0 +/- 0.9 mm, 8.9 +/- 1.0 mm, 13.2 +/- 2.5 mm, 35.9 degrees +/- 5.7 degrees and 31.8 degrees +/- 6.3 degrees, respectively. This study shows that a 40 mm long, 4 to 5 mm diameter screw should be inserted in the lumbar vertebral isthmus at an angle of 30 degrees laterally and anteriorly.

Bone Screws↗